The arrhythmic effects of Na+ and Ca2+ intracellular imbalance were examined on rats with aconitine-induced cardiac arrhythmias. Under conditions of Na(+)-dependent arrhythmogenesis, blockade of Ca(2+)-channels with verapamil aggravated cardiac rhythm disturbances. Correction of ionic imbalance by intravenous injection of calcium preparations in aconitine-induced arrhythmia promoted recovery of stable sinus rhythm and decreased animal mortality. Intracellular imbalance of Na+ and Ca2+ ions can underlie the arrhythmogenic effects of antiarrhythmic drugs.
Pathogenesis of cardiac arrhythmia was determined by EEC changes after ATP-induced complete atrioventricular block. The re-entry mechanism underlays extrasystoles with equal coupling intervals with complexes of ventricular substitution rhythms, which transformed into paroxysmal tachycardia with equal R-R intervals, ventricular flutter, and ventricular fibrillation. Ectopic automaticity was characterized by extrasystole unrelated to the complexes of substitutional rhythms, which was transformed into accelerated idioventricular rhythm and asystole. During trigger activity, the extrasystoles were associated with complexes of basic rhythm and transformed themselves into torsades de pointes and ventricular fibrillation.
We propose a method for experimental modeling of cardiac arrhythmias. The method consists in intravenous injection of LPO inductors: 5% ascorbic acid (50 mg/kg), 1 min later 1% iron sulfate (10 mg/kg), and after the appearance of giant T waves on ECG infusion of 10% calcium chloride in a nonarrhythmogenic dose 100 mg/kg. Cardiac arrhythmias were induced in 100% animals. A significant relationship between increased permeability of erythrocyte membranes and development of fatal cardiac arrhythmias was detected. We assumed that this methodologically simple membrane-destructive model of cardiac arrhythmia is pathogenetically close to arrhythmogenesis in patients with coronary heart disease.
A method for simulating cardiac hypopolarization arrhythmias was developed in order to study changes in cardiomyocyte membrane hypopolarization under the effects of antiarrhythmics and other drugs. The method is based on registration of K(+)-induced arrhythmias after intravenous injection of a minimum arrhythmogenic dose of 1.5% KCl over 2 sec. Atrioventricular and intraventricular blockades without arrhythmias are recorded in first-degree membrane hypopolarization. The same changes and cardiac arrhythmias are characteristic of second-degree hypopolarization. Third degree is associated with transitory cardioplegia, fourth degree with heart arrest and animal death.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.